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Title 

Over-expression of urokinase receptor in human epidermoid-carcinoma cell line (HEp3) increases tumorigenicity on chorio-allantoic membrane and in severe-combined-immunodeficient mice

Authors 

Mi Ae LyuYang Kyu ChoiBo Na ParkByung Joo ParkBum Joon KimIl Kyoo ParkByung Hwa HyunYoon Hoh Kook

Publisher 

Wiley-Blackwell

Issue Date 

1998

Citation 

International Journal of Cancer, vol. 77, no. 0, pp. 257-263

Keywords 

urokinaseurokinase receptorcancer cell culturechorioallantoishumanhuman cellprotein expressionscid mousesquamous cell carcinomacarcinoma, squamous cell

Abstract 

Using chorio-allantoic membranes (CAMs) of chick embryos and severe- combined-immunodeficient (SCID) mice, we investigated the effects of urokinase-type plasminogen-activator receptor (u-PAR) over-expression on the process of invasion and tumorigenicity. By the transfection of u-PAR cDNA, 3 u-PAR-over-expressing clones expressing 1.6- to 4.6-fold more u-PAR mRNA than parent cells were obtained from a human epidermoid-carcinoma cell line, HEp3, that expresses urokinase-type plasminogen activator (u-PA) and u-PAR. All the u-PAR-over-expressing clones showed greater invasiveness (13 to 29%) than that of parent HEp3 cells on CAMs. Immunohistochemistry revealed densely stained u-PAR-positive cells near the margin of the tumor, where a u-PAR- over-expressing clone, designated SM-3, was invading thickened fibrous tissue on CAMs. Three u-PAR-over-expressing clones formed larger tumors (>40 mm3) than did parent HEp3 cells on CAMs. Moreover, when the u-PAR-over-expressing clone (SM-3) was injected s.c. into the back of the SCID mice it produced a larger tumor volume than the control (HEp3) and down-regulated (AS-2) clones and significantly shortened the survival of SCID mice. These results demonstrate that increased u-PAR expression is an important factor in determining the malignant phenotype that makes cancer cells more invasive and tumorigenic.

ISSN 

0020-7136

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2017-04-19


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